Effect of quercetin, genistein and kaempferol on glutathione and glutathione-redox cycle enzymes in 3T3-L1 preadipocytes

Abstract

Context and objective: Many studies have shown that cellular redox potential is largely determined by glutathione (GSH), which accounts for more than 90% of cellular nonprotein thiols. The aim of this study was to delineate the effect of three flavonoids – namely, quercetin, kaempferol and genistein – and exogenous GSH on oxidative damage by the Fenton’s pathway through the GSH and GSH-redox cycle enzymes in 3T3-L1 cells. Materials and methods: 3T3-L1 preadipocytes were exposed to each flavonoid and GSH at concentrations of 0, 5, 10, 15, 20 and 25 µM and then GSH levels and activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rx) and superoxide dismutase (SOD) were measured. Results: Exogenous GSH did not have significant effect on intracellular GSH although slight decrease was observed at 15–25 µM doses. However, each of the three flavonoids sustained intracellular GSH levels in the cells as compared to the respective controls. Quercetin had the most profound effect, followed by kaempferol and genistein in that order. GSH-Px, GSH-Rx and SOD activities increased for all the doses tested compared to their respective controls. Again, quercetin had the maximum increase in enzyme activities followed by kaempferol and genistein for the enzymes tested. Discussion and conclusion: These findings suggest that the flavonoids play an important role in diminishing oxidation-induced biochemical damages. The enhancement of these enzymes may increase the resistance of the organism against oxidative damage by the Fenton’s pathway.

• Flavonoids
• Fenton’s pathway
• glutathione peroxidase
• glutathione reductase
• oxidative damage
• superoxide dismutase

Acknowledgements

The authors thank Mr. Brett Seybert of Tennessee State University for reading and offering his constructive criticisms and suggestions. This study did not involve the use of humans or experimental animals.

Declaration of interest

This study was supported with grants from the Samuel P. Massey Chair of Excellence for Environmental studies chaired by Dr Lonnie Sharpe at the Tennessee State University and that of the Evans-Allen grant to the Tennessee State University from the National Institute of Food and Agriculture (NIFA), of the United States Food and Drug Administration (USFDA). The financial support of the Meharry-Vanderbilt-TSU Cancer Partnership (MVTCP) of the U54 grant number 5U54CA163066 is greatly appreciated.